Paeoniflorin suppresses allergic and inflammatory responses by promoting autophagy in rats with urticaria.
Paeoniflorin suppresses allergic and inflammatory responses by promoting autophagy in rats with urticaria.
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芍药苷通过促进荨麻疹大鼠自噬抑制过敏和炎症反应
DOI：
10.3892/etm.2021.10022
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发表时间：
2021-06
影响因子：
2.7
通讯作者：
Wei Q
中科院分区：
文献类型：
--
作者：
Guo J;Peng L;Zeng J;Zhang M;Xu F;Zhang X;Wei Q
据报道，芍药苷（PF）对几种皮肤病有效，如过敏性接触性皮炎和银屑病;然而，目前尚不清楚PF是否可以预防荨麻疹病变。本研究旨在探讨PF对大鼠荨麻疹皮损的影响及其可能的作用机制。通过使用苏木精-伊红染色的病理学分析，评价PF给药对卵清蛋白诱导的荨麻疹样病变大鼠模型的影响。甲苯胺蓝染色检测肥大细胞，ELISA检测血清组胺水平。PF诱导的自噬活性的调节作用和潜在的潜在机制，这也进行了研究，利用透射电镜，免疫组化和逆转录定量PCR。结果表明，PF抑制过敏和炎症反应，以改善荨麻疹病变，如病理异常，肥大细胞浸润和组胺分泌的衰减所证明的。从机制上讲，发现PF治疗显著限制了炎症细胞因子白细胞介素（IL）-23的产生和释放，而IL-17的水平保持不变。PF干预导致自噬体数量增加，沿着轻链3B（LC 3B）和Beclin-1水平升高，P62水平降低，表明PF可增强荨麻疹病变中的自噬活性。PF处理后，肝激酶B1（LKB 1）和AMP活化蛋白激酶-α（AMPK-α）的表达增加，这与PF增强自噬活性有关。结论：PF可通过抑制炎性细胞因子IL-23，增强LKB 1/AMPK-α通路的自噬活性，有效改善荨麻疹病变。
Paeoniflorin (PF) has been reported to be effective against several skin disorders, such as allergic contact dermatitis and psoriasis; however, it remains unclear whether PF can protect against urticarial lesions. Herein, the effects of PF on rats with urticarial lesions and the possible underlying mechanism were investigated. The effects of PF administration on a rat model of ovalbumin-induced urticarial-like lesions were evaluated via pathological analysis using hematoxylin-eosin staining. Toluidine blue staining was performed to detect mast cells and ELISA was performed to determine serum histamine levels. PF-induced regulatory effects on autophagic activity and the potential underlying mechanism of this were also investigated using transmission electron microscopy, immunohistochemistry and reverse transcription-quantitative PCR. It was demonstrated that PF suppressed allergic and inflammatory responses to improve urticarial lesions, as evidenced by the attenuation of pathological abnormalities, mast cell infiltration and histamine secretion. Mechanistically, PF treatment was found to markedly limit the production and release of inflammatory cytokine interleukin (IL)-23, while the levels of IL-17 remained unchanged. PF intervention led to an increased number of autophagosomes, along with higher levels of light chain 3B (LC3B) and Beclin-1, and lower levels of P62, indicating that PF could augment autophagic activity in urticarial lesions. PF treatment increased the expression of liver kinase B1 (LKB1) and AMP-activated protein kinase-α (AMPK-α), contributing to the PF-enhanced autophagic activity. In conclusion, PF could effectively improve urticarial lesions by inhibiting inflammatory cytokine IL-23 and increasing the autophagic activity via the LKB1/AMPK-α pathway.
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影响因子：
13.3
作者：
Rai S;Arasteh M;Jefferson M;Pearson T;Wang Y;Zhang W;Bicsak B;Divekar D;Powell PP;Naumann R;Beraza N;Carding SR;Florey O;Mayer U;Wileman T
通讯作者：
Wileman T
影响因子：
4.8
作者：
Lee, James;Rodero, Mathieu Paul;Khosrotehrani, Kiarash
通讯作者：
Khosrotehrani, Kiarash
影响因子：
10.9
作者：
Feldmeyer, Laurence;Mylonas, Alessio;Conrad, Curdin
通讯作者：
Conrad, Curdin
影响因子：
14.2
作者：
Larsen, Jeppe Madura;Bonefeld, Charlotte Menne;Skov, Lone
通讯作者：
Skov, Lone
DOI：
10.4049/jimmunol.1800013
发表时间：
2018-09-15
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Hawkes JE;Yan BY;Chan TC;Krueger JG
通讯作者：
Krueger JG